Institution
Kettering University
Education•Flint, Michigan, United States•
About: Kettering University is a education organization based out in Flint, Michigan, United States. It is known for research contribution in the topics: Cancer & RNA. The organization has 6842 authors who have published 7689 publications receiving 337503 citations. The organization is also known as: GMI Engineering & Management Institute & General Motors Institute.
Topics: Cancer, RNA, Antigen, DNA, Population
Papers published on a yearly basis
Papers
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155 citations
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TL;DR: Theoretical relationships have been drawn between acoustic emission (AE) and the metal cutting process parameters by relating the energy content of the AE signal to the plastic work of deformation which generates the emission signals as mentioned in this paper.
Abstract: Theoretical relationships have been drawn between acoustic emission (AE) and the metal cutting process parameters by relating the energy content of the AE signal to the plastic work of deformation which generates the emission signals The RMS value of the emission signal is expressed in terms of the basic cutting parameters Results are presented for 6061-T6 aluminum and SAE 1018 steel over the range of speeds 252 to 372 sfm (0128 to 19 m/s) and rake angles 10 to 40 deg Good correlation has been found between predicted and experimental signal energy levels In addition, AE generation from chip contact along the tool face is studied and the AE energy level reflects the existence of chip sticking and sliding on the tool face, and indicates the feasibility of utilizing AE in tool wear sensing
155 citations
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TL;DR: It is shown that loss of function of mouse Mks1 results in an accurate model of human MKS, with structural abnormalities in the neural tube, biliary duct, limb patterning, bone development and the kidney that mirror the human syndrome.
Abstract: Meckel syndrome (MKS) is a rare autosomal recessive disease causing perinatal lethality associated with a complex syndrome that includes occipital meningoencephalocele, hepatic biliary ductal plate malformation, postaxial polydactyly and polycystic kidneys. The gene mutated in type 1 MKS encodes a protein associated with the base of the cilium in vertebrates and nematodes. However, shRNA knockdown studies in cell culture have reported conflicting results on the role of Mks1 in ciliogenesis. Here we show that loss of function of mouse Mks1 results in an accurate model of human MKS, with structural abnormalities in the neural tube, biliary duct, limb patterning, bone development and the kidney that mirror the human syndrome. In contrast to cell culture studies, loss of Mks1 in vivo does not interfere with apical localization of epithelial basal bodies but rather leads to defective cilia formation in most, but not all, tissues. Analysis of patterning in the neural tube and the limb demonstrates altered Hedgehog (Hh) pathway signaling underlies some MKS defects, although both tissues show an expansion of the domain of response to Shh signaling, unlike the phenotypes seen in other mutants with cilia loss. Other defects in the skull, lung, rib cage and long bones are likely to be the result of the disruption of Hh signaling, and the basis of defects in the liver and kidney require further analysis. Thus the disruption of Hh signaling can explain many, but not all, of the defects caused by loss of Mks1.
154 citations
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05 Jun 2006TL;DR: In this paper, an exploratory numerical study of the control of transitional and turbulent separated flows by means of asymmetric dielectric-barrier discharge (DBD) actuators is presented.
Abstract: : An exploratory numerical study of the control of transitional and turbulent separated flows by means of asymmetric dielectric-barrier-discharge (DBD) actuators is presented. The flow fields are simulated employing an extensively validated high-fidelity Navier-Stokes solver which is augmented with both phenomenological and first-principles models representing the plasma-induced body forces imparted by the actuator on the fluid. Several applications are considered, including suppression of wing stall, control of boundary layer transition on a plate, control of laminar separation over a ramp, and turbulent separation over a wall-mounted hump. Effective suppression of stall over a NACA 0015 airfoil at moderate Reynolds numbers is demonstrated using either co-flow or counter-flow pulsed actuators with sufficiently high frequency. By contrast, continuous actuation (simulated by a steady body force in the phenomenological model) is found to provide little control of separation. For continuous actuator operation, the first-principles approach is needed in order to reproduce the benefits of the inherently unsteady force induced by the plasma actuator. The pulsed-modulated unsteady plasma force is found to be more effective than a monochromatic radio-frequency forcing. These results highlight the greater importance of transition and turbulence enhancement mechanisms rather than pure wall-jet momentum injection for the effective use of DBD devices. As a consequence, meaningful computations require the use of three-dimensional large-eddy simulation approaches capable of capturing the effects of unsteady forcing on the transitional/turbulent flow structure. For a laminar boundary layer developing along a flat plate, a counter-flow DBD actuator is shown to provide an effective on-demand tripping device.
153 citations
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University of Oxford1, Anthony Nolan2, Ludwig Maximilian University of Munich3, Biomedical Primate Research Centre4, Kettering University5, Hoffmann-La Roche6, Fred Hutchinson Cancer Research Center7, University of Geneva8, University of Vienna9, Stanford University10, Kyushu University11, Leiden University Medical Center12, Harvard University13, University of California, Los Angeles14
TL;DR: The list of genes in the HLA region is given in Table 1.1 as mentioned in this paper and the change of name of the gene HLADNA to HLA-DOA, as published in the monthly updates, was confirmed, following further results showing that the gene codes for the alpha chain associated with HLA DOB.
Abstract: 1. The Naming of New Genes Within the HLA Region The Committee agreed in 1996 to defer the naming of new genes within the HLA region. However, in view of the great interest and work being carried out on the MIC (MHC Class I chain related) genes, already named by the Human Genome Nomenclature Committee as MICA, MICB, MICC, MICD and MICE in April and September 1994 [15, 16], it was agreed that they should be included within the official HLA nomenclature for the purpose of naming alleles of these genes. In addition the change of name of the gene HLADNA to HLA-DOA, as published in the monthly updates, was confirmed, following further results showing that the gene codes for the alpha chain associated with HLA-DOB. The updated list of genes in the HLA region is given in Table 1.
153 citations
Authors
Showing all 6853 results
Name | H-index | Papers | Citations |
---|---|---|---|
Joan Massagué | 189 | 408 | 149951 |
Chris Sander | 178 | 713 | 233287 |
Timothy A. Springer | 167 | 669 | 122421 |
Murray F. Brennan | 161 | 925 | 97087 |
Charles M. Rice | 154 | 561 | 83812 |
Lloyd J. Old | 152 | 775 | 101377 |
Howard I. Scher | 151 | 944 | 101737 |
Paul Tempst | 148 | 309 | 89225 |
Pier Paolo Pandolfi | 146 | 529 | 88334 |
Barton F. Haynes | 144 | 911 | 79014 |
Jedd D. Wolchok | 140 | 713 | 123336 |
James P. Allison | 137 | 483 | 83336 |
Harold E. Varmus | 137 | 496 | 76320 |
Scott W. Lowe | 134 | 396 | 89376 |
David S. Klimstra | 133 | 564 | 61682 |